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Dr. Somak Mazumdar

Introduction

By definition, amblyopia is decreased best corrected visual acuity due to deprived form vision and/or abnormal binocular interaction without any organic (pathological) cause of the eye. The most common form of amblyopia is anisometropia where refractive error plays the key factor. But in spite of refractive error correction the visual outcome remains often poor.

This indicates that there may be some unrevealed factors present which dictates the visual deprivationand outcome in anisometropic amblyopia. This may be pathological. As more and more newer technologies are available now-a-days, search of organic causes in anisometropic amblyopia is becoming quite desirable. The main areas of interest for such problems are macula, optic nerve head and Retinal Nerve Fibre Layer (RNFL). So, investigating these three, may enlighten some occult features.

Macula and RNFL are best analysed by optical coherence tomography (OCT). For this, third generation spectral (Fourier) domain system (SDOCT) is ideal. On the other hand, optic nerve head (ONH) function is best evaluated with automated perimetry (AP). So combination of these three methods yields best result regarding evaluation of macula-ONH-nerve fibres. Now as we know anisometropic amblyopia maintain normal anatomy except change in axial length – there may be some subtle, underlying derangement present in macula or ONH or in RNFL in those eyes. The primary suspicion was probable macular morpho-anatomical change and foveal sensitivity alteration. Combined SDOCT and AP thus found best evaluating tool there.

Purpose

Purpose of this study was to find out the macular morphology, visual field pattern, foveal threshold sensitivity and retinal nerve fibre layer (RNFL) changes in anisometropic amblyopic eyes – to rule out any true organic cause.

Materials and Methods

This was a retrospective analysis of 120 pure anisometropic amblyopic eyes who came to our tertiary care hospital. The duration of the study was 9 months.

The inclusion criteria were: (1) any degree anisometropic amblyopia (either unilateral or bilateral), (2) age 18 years or more and (3) best corrected visual acuity (BCVA) 6/60 (20/200) or better. The reason behind choice of such age group was lack of normative data base in Humphery visual field (HVF) analyser and RNFL analyser. These two have a dataset which lacks information of age group less than 18 years. Moreover, HVF analysis requires at least 6/60 vision.

The excluded categories were any other type of amblyopia, age less than 18 years, any other pre-existing disease with field defect (glaucomatous or neuronal) and pre-existing macular pathology.

Regarding the assessment of best corrected visual acuity (BCVA) and IOP -bothqualitative (type) and quantitative (amount) status of refractive error was evaluated. The eyes were divided into myopic and hyperopic category accordingly. Then the spherical power (Dioptre sphere or DS) was calculated and for cylindrical power (Dioptre cylinder or DC) – the spherical equivalent was taken into consideration.This was done to avoid any axis related complication. So, the final refractive power was basically a combination of both (DS + DC/2).

Then all patients underwent 3 major investigations. The 1st investigation was spectral domain OCT (SD-OCT) evaluation of the macula. The 3rd generation SDOCT is now the most widely used investigating tool to assess macular morpho-anatomy. This is because it is non-invasive, rather cost effective, devoid of any side effect and nearly correlates histo-anatomical features in situ. The ultra-structures of neurosensory retina (NSR), photoreceptor layers and RPE were clearly delineated on SDOCT.

Another advantage of OCT is that it gives measurement of foveal thickness or popularly called central foveal thickness (CFT). Any alteration of foveal anatomy is practically detected by the value of CFT; more than normal indicates hypertrophy and less means atrophy. Normal CFT in Indian eyes is 240 ± 20 micron. CFT less than 220 micron was taken as atrophy and more than 260 micron was hypertrophy of the Neuro Sensory Retina (NSR).

The 2nd investigation done was Humphery visual field (HVF) analysis. All patients undergone this automated perimetry (AP) field assessment and subsequent foveal sensitivity was measured in dB or decibel. The 30-2, SITA-standard, stimulus III method of field analysis was used. Any field defect and change in foveal threshold/ sensitivity was observed on AP.

The 3rd investigation was RNFL analysis done again with OCT. The status of nerve fibre was assessed accordingly and divided into ‘within normal limit’ and ‘outside normal limit’ category. Basically, quadrant wise thinning was assessed by the software and converted into results like that.

Results

The mean BCVA detected was 0.65 log MAR[range 0.3-1.0] equivalent to 6/30 Snellen’s visual acuity. Most patients had myopia (72.5%; 87/120 eyes). Hyperopic amblyopia accounted less. Now, surprisingly 55% of all amblyopic eyes showed significant macular pathological changes. Rest were within normal limit. The affected 66 eyes had clear foveal alteration in macula detected on OCT (Table 1). It showed foveal NSR atrophy in 39.1% (47/120) eyes and hypertrophy in 19/120 eyes (15.8%). Irregularities like atrophy and disruption at photoreceptors layer (inner-outer segment junction on OCT) were found in 31/120 eyes (25.8%). In two eyes the photoreceptors were found lost. RPE alteration was present in 7/120 eyes (5.8%).

Table 1. OCT based Foveo-Macular alteration

Morpho-anatomy Eyes Rate of involvement (%)
Foveal NSR atrophy 47/120 39.1
Foveal NSR hypertrophy 19/120 15.8
Photoreceptor irregularities 31/120 25.8
RPE alteration 7/120 5.8

Mean CFT was found 215.8 microns [range 56-374]. Visual fields were found mostly normal. In 68/120 (56.7%) eyes, the AP (30-2) showed no significant change. But,in 43.3% (52/120) eyes, there was detectablescotomatous effect. The different scotomas we found are depicted in Table 2.

Table 2. Scotomas on AP (30-2)

Types Eyes
Central scotoma 14/120
Peripheral scotoma 12/120
Generalised depression 12/120
Arcuate scotoma 13/120

 

Again69% (83/120 eyes) showed diminished foveal sensitivity, measuring a value <30 dB. Mean sensitivity was 26.5 dB [range 11-38; Table 3]. Rest 31% had normal fovea with normal threshold.

Table 3. Foveal sensitivity on AP (30-2)

Foveal threshold (dB) Eyes
Upto 30 (normal) 31%
<30(subnormal) 69%

RNFL analysis showed 17.5% (21/120) eyes had definite nerve fiber loss and subsequent thinning. Thus, outside normal limit.

Table 4. RNFL assessment

RNFL Eyes
Outside normal limit 17.5%
Within normal limit 83.5%

 

Discussion

Anisometropic amblyopia (AA) is still a challenge to the physician. This is because of its enigmatic behaviour. As we know, the traditional concept of amblyopia says – there should not be any detectable organic cause or pathology. The only obvious problem is refractive error. But we all know that mere refractive error correction may not be enough for AA. There is always some residual visual deficit remains and for which there is no solution available. If detected early on 1st decade, therapy yields good visual recovery. But as age advances the problem becomes more irreversible. This had raised the question to our mind, why in spite of proper treatment some eyes never get good visual regain?

To our suspicion, the macula has a definite role in anisometropic amblyopia. This is probably the most important yet grey zone. Spectral domain OCT now delineates macular morpho-anatomy in a distinct way. We evaluated macula thoroughly with SDOCT and to our utmost surprise most of it found subnormal. Contradicting the popular belief, more than half of total anisometropic amblyopic eye had shown altered morpho-anatomy of macula. What we found that in nearly 3/4th of affected macula had a neurosensory atrophy. This, definitely an irreversible situation. Also disrupted photoreceptors were detected in 1/4th of eyes. This again complicated the pathology.

Therefore two definite causes were revealed which were practically untreatable. Another 1/4th eyes had hypertrophy of neurosensory macula. As both myopes and hyperopes were found in this category, any direct cause-effect association was not detected. RPE alteration was insignificant. But it was obvious that all layers of macula were involved in anisometropic amblyopia.

Now analysis of central foveal thickness (CFT) showed that the mean value indicated atrophy of macula. Almosthalf of anisometropic amblyopic eyes had subnormal thickness of macula. Nearly 1/5th of eyes had CFT less than 200 micron which indicated advanced atrophy.

When we gathered the automated perimetry dataset we found more than half of the patients had normal response. But44% of the total amblyopic eyes had some degrees of scotoma. Of course, foveal threshold noted grossly diminished in almost 2/3rd of all amblyopic eyes. This was shocking and added another irreversible scenario into the disease process. The mean foveal threshold was noticed much less of normal value.

RNFL analysis showed 1/5th eyes had neuronal thinning. This, along with changes in visual field and foveal sensitivity contributes probably in the formation of amblyopia. Obviously, these are irreversible.

Thepresent study is correlating with the previous observations. But this study has some differences with other. First, in the other studies, the average sample sizes were less than 50. Here the size is more than 100 and that indicates a significant number. Secondly, earlier all types of amblyopia were evaluated in a mixture. Here only one and most common clinical type was targeted. So, results are more precise. Third, the causes of resistant visual deficit were not pinpointed in previous studies. Here at least three causes – namely foveal atrophic changes, loss of nerve fibre layer and decreased foveal sensitivity were found. Being irreversible changes, it indicated why sometimes anisometropic amblyopia never gets cured. Therefore, prognosis found more explainable. But definitely more elaborate study is required to assess all aspects of anisometropic amblyopia.

Conclusion

So, to conclude, eyes with anisometropic amblyopia may have altered macular anatomy and diminished foveal sensitivity that could be organic in nature and difficult to treat. Also thinning of retinal nerve fibre layer added some more complications into the already complex disease process. Combination of all these results in a poorer outcome even with proper treatment. Spectral Domain OCT and Automated Perimetryboth have a significant role to detect this.

References

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